Table 2.
The promoting effects of ROS in cancer
| Function | Result | Effect |
|---|---|---|
| Oxidize nucleobases | Form oxidative damage products | DNA mutation, subsequently promoting cancer formation |
| BRCA2 degradation | Inhibit BRCA2 | |
| Oxidize hOGG1 | Inhibit hOGG1 activity | |
| Stabilize HIF-1α | Interfere with T-cell development | Inhibit T cell function, finally promoting cancer development and metastasis. |
| Reduce CD3ζ chain expression | Block T cells differentiation and activation | |
| Phosphorylate ERK | T cells apoptosis | |
| Downregulate CD16ζ expression | Inhibit NK cells cytotoxicity | Inhibit NK cell function, subsequently promoting tumor growth and metastasis |
| Attenuate eIF-2B phosphorylation | Suppress ADCC of NK cell | |
| Inactivate PTEN | Macrophage recruitment, M2 polarization of macrophage | Promote tumor growth, invasion and metastasis |
| Activate TNF-α/TNFR1 | ||
| Activate NF-κB | Lose cell-cell junction | Trigger EMT process in cancer cells, finally promoting cancer cell invasion and metastasis |
| Promote TGF-β expression | ||
| Activate HIF-1α | ||
| Cause KEAP1 degradation | ||
| Activate PI3K/Akt | ||
| Oxidize 14-3-3ζ | Cytoskeleton remodeling | |
| Induce Arp2/3 recruitment | ||
| Inhibit protein tyrosine phosphatase | ||
| Activate MAPK, AP-1 and NF-κB | ECM degradation |